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  • Frontiers Media SA  (23)
  • Wang, Li  (23)
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  • Frontiers Media SA  (23)
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  • 1
    Online Resource
    Online Resource
    DataSheet_2.docx
    Frontiers Media SA ; 2022
    In:  Frontiers in Oncology Vol. 12 ( 2022-7-14)
    Details
    In: Frontiers in Oncology, Frontiers Media SA, Vol. 12 ( 2022-7-14)
    Abstract: Helicobacter pylori ( H. pylori )-derived vacuolating cytotoxin A (VacA) causes damage to various organelles, including mitochondria, and induces autophagy and cell death. However, it is unknown whether VacA-induced mitochondrial damage can develop into mitophagy. In this study, we found that H. pylori , H. pylori culture filtrate (HPCF), and VacA could activate autophagy in a gastric epithelial cell line (GES-1). VacA-caused mitochondrial depolarization retards the import of PINK1 into the damaged mitochondria and evokes mitophagy. And, among mass spectrometry (LC-MS/MS) identified 25 mitochondrial proteins bound with VacA, Tom20, Tom40, and Tom70, TOM complexes responsible for PINK1 import, were further identified as having the ability to bind VacA in vitro using pull-down assay, co-immunoprecipitation, and protein–protein docking. Additionally, we found that the cell membrane protein STOM and the mitochondrial inner membrane protein PGAM5 also interacted with VacA. These findings suggest that VacA captured by STOM forms endosomes to enter cells and target mitochondria. Then, VacA is transported into the mitochondrial membrane space through the TOM complexes, and PGAM5 aids in inserting VacA into the inner mitochondrial membrane to destroy the membrane potential, which promotes PINK1 accumulation and Parkin recruitment to induce mitophagy. This study helps us understand VacA entering mitochondria to induce the mitophagy process.
    Type of Medium: Online Resource
    ISSN: 2234-943X
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fonc.2022.881829
    DOI: 10.3389/fonc.2022.881829.s001
    DOI: 10.3389/fonc.2022.881829.s002
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2649216-7
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  • 2
    Online Resource
    Online Resource
    Presentation_1.pdf
    Frontiers Media SA ; 2022
    In:  Frontiers in Oncology Vol. 12 ( 2022-10-24)
    Details
    In: Frontiers in Oncology, Frontiers Media SA, Vol. 12 ( 2022-10-24)
    Abstract: Although arsenic trioxide (ATO) shows a strong anti-tumor effect in the treatment of acute promyelocytic leukemia, it does not benefit patients with hepatocellular carcinoma (HCC). Thus, combination therapy is proposed to enhance the efficacy of ATO. Parthenolide (PTL), a natural compound, selectively eradicates cancer cells and cancer stem cells with no toxicity to normal cells. In this study, we chose PTL and ATO in combination and found that nontoxic dosage of PTL and ATO co-treatment can synergistically inhibit the in vitro and in vivo proliferation activity of HCC cells through suppressing stemness and self-renewal ability and inducing mitochondria-dependent apoptosis. More importantly, USP7-HUWE1-p53 pathway is involved in PTL enhancing ATO-induced apoptosis of HCC cell lines. Meanwhile, accompanied by induction of apoptosis, PTL and ATO evoke autophagic activity via inhibiting PI3K/Akt/mTOR pathway, and consciously controlling autophagy can improve the anti-HCC efficacy of a combination of PTL and ATO. In short, our conclusion represents a novel promising approach to the treatment of HCC.
    Type of Medium: Online Resource
    ISSN: 2234-943X
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fonc.2022.988528
    DOI: 10.3389/fonc.2022.988528.s001
    DOI: 10.3389/fonc.2022.988528.s002
    DOI: 10.3389/fonc.2022.988528.s003
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2649216-7
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  • 3
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    A Single L/D-Substitution at Q4 of the mInsA2-10 Epitope Prevents Type 1 Diabetes in Humanized NOD Mice
    Frontiers Media SA ; 2021
    In:  Frontiers in Immunology Vol. 12 ( 2021-8-30)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2021-8-30)
    Abstract: Autoreactive CD8 + T cells play an indispensable key role in the destruction of pancreatic islet β-cells and the initiation of type 1 diabetes (T1D). Insulin is an essential β-cell autoantigen in T1D. An HLA-A*0201-restricted epitope of insulin A chain (mInsA 2-10 ) is an immunodominant ligand for autoreactive CD8 + T cells in NOD. β2m null . HHD mice. Altered peptide ligands (APLs) carrying amino acid substitutions at T cell receptor (TCR) contact positions within an epitope are potential to modulate autoimmune responses via triggering altered TCR signaling. Here, we used a molecular simulation strategy to guide the generation of APL candidates by substitution of L-amino acids with D-amino acids at potential TCR contact residues (positions 4 and 6) of mInsA 2-10 , named mInsA 2-10 DQ4 and mInsA 2-10 DC6, respectively. We found that administration of mInsA 2-10 DQ4, but not DC6, significantly suppressed the development of T1D in NOD. β2m null . HHD mice. Mechanistically, treatment with mInsA 2-10 DQ4 not only notably eliminated mInsA 2-10 autoreactive CD8 + T cell responses but also prevented the infiltration of CD4 + T and CD8 + T cells, as well as the inflammatory responses in the pancreas of NOD. β2m null .HHD mice. This study provides a new strategy for the development of APL vaccines for T1D prevention.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    DOI: 10.3389/fimmu.2021.713276
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2606827-8
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  • 4
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    Recent and current advances in PET/CT imaging in the field of predicting epidermal growth factor receptor mutations in non-small cell lung cancer
    Frontiers Media SA ; 2022
    In:  Frontiers in Oncology Vol. 12 ( 2022-10-6)
    Details
    In: Frontiers in Oncology, Frontiers Media SA, Vol. 12 ( 2022-10-6)
    Abstract: Tyrosine kinase inhibitors (TKIs) are a significant treatment strategy for the management of non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) mutation status. Currently, EGFR mutation status is established based on tumor tissue acquired by biopsy or resection, so there is a compelling need to develop non-invasive, rapid, and accurate gene mutation detection methods. Non-invasive molecular imaging, such as positron emission tomography/computed tomography (PET/CT), has been widely applied to obtain the tumor molecular and genomic features for NSCLC treatment. Recent studies have shown that PET/CT can precisely quantify EGFR mutation status in NSCLC patients for precision therapy. This review article discusses PET/CT advances in predicting EGFR mutation status in NSCLC and their clinical usefulness.
    Type of Medium: Online Resource
    ISSN: 2234-943X
    URL: Article
    DOI: 10.3389/fonc.2022.879341
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2649216-7
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  • 5
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    Table_1.PDF
    Frontiers Media SA ; 2018
    In:  Frontiers in Microbiology Vol. 9 ( 2018-6-14)
    Details
    In: Frontiers in Microbiology, Frontiers Media SA, Vol. 9 ( 2018-6-14)
    Type of Medium: Online Resource
    ISSN: 1664-302X
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fmicb.2018.01262
    DOI: 10.3389/fmicb.2018.01262.s001
    DOI: 10.3389/fmicb.2018.01262.s002
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2018
    detail.hit.zdb_id: 2587354-4
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  • 6
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    Online Resource
    IRF7: role and regulation in immunity and autoimmunity
    Frontiers Media SA ; 2023
    In:  Frontiers in Immunology Vol. 14 ( 2023-8-10)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 14 ( 2023-8-10)
    Abstract: Interferon regulatory factor (IRF) 7 was originally identified as master transcriptional factor that produced IFN-I and regulated innate immune response, subsequent studies have revealed that IRF7 performs a multifaceted and versatile functions in multiple biological processes. In this review, we provide a comprehensive overview on the current knowledge of the role of IRF7 in immunity and autoimmunity. We focus on the latest regulatory mechanisms of IRF7 in IFN-I, including signaling pathways, transcription, translation, and post-translational levels, the dimerization and nuclear translocation, and the role of IRF7 in IFN-III and COVID-19. In addition to antiviral immunity, we also discuss the role and mechanism of IRF7 in autoimmunity, and the further research will expand our understanding of IRF7.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    DOI: 10.3389/fimmu.2023.1236923
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2606827-8
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  • 7
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    Data_Sheet_1.PDF
    Frontiers Media SA ; 2022
    In:  Frontiers in Pediatrics Vol. 10 ( 2022-6-22)
    Details
    In: Frontiers in Pediatrics, Frontiers Media SA, Vol. 10 ( 2022-6-22)
    Abstract: The precise genetic diagnosis of a sarcoglycanopathy or dystrophinopathy is sometimes extremely challenging, as pathogenic non-coding variants and/or complex structural variants do exist in DMD or sarcoglycan genes. This study aimed to determine the genetic diagnosis of three patients from two unrelated families with a suspected sarcoglycanopathy or dystrophinopathy based on their clinical, radiological, and pathological features, for whom routine genomic detection approaches failed to yield a definite genetic diagnosis. Methods Muscle-derived reverse transcription-polymerase chain reaction analysis and/or TA cloning of DMD , SGCA , SGCB , SGCD , and SGCG mRNA were performed to identify aberrant transcripts. Genomic Sanger sequencing around the aberrant transcripts was performed to detect possible splice-altering variants. Bioinformatic and segregation studies of the detected genomic variants were performed in both families. Results In patients F1-II1 and F1-II2, we identified two novel pathogenic compound heterozygous variants in SGCB . One is a deep intronic splice-altering variant (DISV), c.243 + 1558C & gt; T in intron 2 causing the activation of an 87-base pair (bp) pseudoexon, and the other one is a non-canonical splicing site variant, c.243 + 6T & gt; A leading to the partial intron inclusion of 10-bp sequence. A novel DISV, c.243 + 1576C & gt; G causing a 106-bp pseudoexon activation, and a nonsense variant in SGCB were identified in compound heterozygous state in patient F2-II1. Unexpectedly, the predicted nonsense variant, c.334C & gt; T in exon 3, created a new donor splice site in exon 3 that was stronger than the natural one, resulting in a 97-bp deletion of exon 3 (r.333_429del). Conclusion This is the first identification of rare exonic and DISVs in the SGCB gene.
    Type of Medium: Online Resource
    ISSN: 2296-2360
    URL: Article
    URL: Article
    DOI: 10.3389/fped.2022.900280
    DOI: 10.3389/fped.2022.900280.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2711999-3
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  • 8
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    Table_7.xlsx
    Frontiers Media SA ; 2022
    In:  Frontiers in Endocrinology Vol. 13 ( 2022-12-5)
    Details
    In: Frontiers in Endocrinology, Frontiers Media SA, Vol. 13 ( 2022-12-5)
    Abstract: Epidemiological studies have suggested that dietary factors, especially high consumption of high glycaemic index carbohydrates and sugars, may trigger or exacerbate the progression of type 1 diabetes. We aimed to provide experimental evidence to confirm this relevance and to explore the underlying mechanisms. Methods NOD mice were given sustained high-glucose drinking or glucose-free water and observed for the incidence of type 1 diabetes and islet inflammation. RNAseq was performed to detect the transcriptome changes of the NOD islet beta cell line NIT-1 after high glucose treatment, and mass spectrometry was performed to detect the proteome changes of NIT-1-cells-derived sEVs. Results Sustained high glucose drinking significantly aggravates islet inflammation and accelerates the onset of type 1 diabetes in NOD mice. Mechanistically, high glucose treatment induces aberrant ER stress and up-regulates the expression of autoantigens in islet beta cell. Moreover, high glucose treatment alters the proteome of beta-cells-derived sEVs, and significantly enhances the ability of sEVs to promote DC maturation and stimulate immune inflammatory response. Discussion This study provides evidence for negative effect of high glucose intake as a dietary factor on the pathogenesis of type 1 diabetes in genetically predisposed individuals. Therefore, avoiding high sugar intake may be an effective disease prevention strategy for children or adults susceptible to type 1 diabetes.
    Type of Medium: Online Resource
    ISSN: 1664-2392
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fendo.2022.1037822
    DOI: 10.3389/fendo.2022.1037822.s001
    DOI: 10.3389/fendo.2022.1037822.s002
    DOI: 10.3389/fendo.2022.1037822.s003
    DOI: 10.3389/fendo.2022.1037822.s004
    DOI: 10.3389/fendo.2022.1037822.s005
    DOI: 10.3389/fendo.2022.1037822.s006
    DOI: 10.3389/fendo.2022.1037822.s007
    DOI: 10.3389/fendo.2022.1037822.s008
    DOI: 10.3389/fendo.2022.1037822.s009
    DOI: 10.3389/fendo.2022.1037822.s010
    DOI: 10.3389/fendo.2022.1037822.s011
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2592084-4
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  • 9
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    Predictors of long-term decannulation in patients with disorders of consciousness
    Frontiers Media SA ; 2023
    In:  Frontiers in Neurology Vol. 14 ( 2023-10-2)
    Details
    In: Frontiers in Neurology, Frontiers Media SA, Vol. 14 ( 2023-10-2)
    Abstract: The predictors of tracheostomy decannulation in patients with disorders of consciousness (DOC) are not comprehensively understood, making prognosis difficult. The primary objective of this study was to identify predictors of tracheostomy decannulation in patients with disorders of consciousness (DOC). The secondary aim was to evaluate the feasibility and safety of the modified Evans blue dye test (MEBDT) in tracheostomized DOC patients. Methods This retrospective study included all patients with disorders of consciousness (DOC) who underwent tracheostomy and were admitted between January 2016 and September 2022. Age, sex, etiology, initial Glasgow coma scale (GCS), initial Coma Recovery Scale-Revised (CRS-R), diagnosis of unresponsive wakefulness syndrome (UWS) or minimal consciousness state (MCS), MEBDT, initial modified Rankin scale (mRS), and initial Functional Oral Intake Scale (FOIS) were collected upon study enrollment. The relationship between clinical characteristics and cannulation status was investigated through a Cox regression model. Results A total of 141 patients were included in the study. The average age of these patients was 52.5 ± 16.7 years, with 42 (29.8%) being women. During the study period, 86 subjects (61%) underwent successful decannulation. Univariate analysis revealed that decannulated patients exhibited a significantly better conscious state compared to those without decannulation (CRS-R: p   & lt; 0.001; GCS: p  = 0.023; MCS vs. UWS: p   & lt; 0.001). Additionally, a negative modified Evans blue dye test (MEBDT) result was significantly associated with tracheostomy decannulation ( p   & lt; 0.001). In the multivariate analysis, successful decannulation was associated with a higher level of consciousness (MCS vs. UWS, p   & lt; 0.001, HR = 6.694) and a negative MEBDT result (negative vs. positive, p  = 0.006, HR = 1.873). The Kaplan–Meier analysis further demonstrated that MEBDT-negative patients and those in the MCS category had a higher probability of decannulation at 12 months ( p   & lt; 0.001). Conclusion The findings of this study indicate that a negative MEBDT result and a higher level of consciousness can serve as predictive factors for successful tracheostomy decannulation in DOC patients.
    Type of Medium: Online Resource
    ISSN: 1664-2295
    URL: Article
    DOI: 10.3389/fneur.2023.1099307
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2564214-5
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  • 10
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    Table_1.DOCX
    Frontiers Media SA ; 2019
    In:  Frontiers in Neurology Vol. 10 ( 2019-9-20)
    Details
    In: Frontiers in Neurology, Frontiers Media SA, Vol. 10 ( 2019-9-20)
    Type of Medium: Online Resource
    ISSN: 1664-2295
    URL: Article
    URL: Article
    DOI: 10.3389/fneur.2019.00995
    DOI: 10.3389/fneur.2019.00995.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2019
    detail.hit.zdb_id: 2564214-5
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